Mack V, Burnashev N, Kaiser K M, Rozov A, Jensen V, Hvalby O, Seeburg P H, Sakmann B, Sprengel R
Department of Molecular Neurobiology, Max-Planck-Institute for Medical Research, D-69120 Heidelberg, Germany.
Science. 2001 Jun 29;292(5526):2501-4. doi: 10.1126/science.1059365.
Plasticity of mature hippocampal CA1 synapses is dependent on l-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) receptors containing the glutamate receptor A (GluR-A) subunit. In GluR-A-deficient mice, plasticity could be restored by controlled expression of green fluorescent protein (GFP)-tagged GluR-A, which contributes to channel formation and displayed the developmental redistribution of AMPA receptors in CA1 pyramidal neurons. Long-term potentiation (LTP) induced by pairing or tetanic stimulation was rescued in adult GluR-A(-/-) mice when (GFP)GluR-A expression was constitutive or induced in already fully developed pyramidal cells. This shows that GluR-A-independent forms of synaptic plasticity can mediate the establishment of mature hippocampal circuits that are prebuilt to express GluR-A-dependent LTP.
成熟海马体CA1突触的可塑性依赖于含有谷氨酸受体A(GluR-A)亚基的L-α-氨基-3-羟基-5-甲基异恶唑-4-丙酸(AMPA)受体。在GluR-A缺陷型小鼠中,通过绿色荧光蛋白(GFP)标记的GluR-A的可控表达可恢复可塑性,该蛋白有助于通道形成并显示了AMPA受体在CA1锥体神经元中的发育性重新分布。当(GFP)GluR-A表达为组成型或在已完全发育的锥体细胞中诱导表达时,成年GluR-A(-/-)小鼠中由配对或强直刺激诱导的长时程增强(LTP)得以挽救。这表明不依赖GluR-A的突触可塑性形式可以介导成熟海马体回路的建立,这些回路预先构建以表达依赖GluR-A的LTP。